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Lnc-NLC1-C inhibits migration, invasion and autophagy of glioma cells by targeting miR-383 and regulating PRDX-3 expression.

ABSTRACT: Long non-coding RNAs (lncRNAs) serve an important role in tumor progression, and their abnormal expression is associated with tumor development. The lncRNA narcolepsy candidate region 1 gene C (lnc-NLC1-C) is involved in numerous types of cancer, but its biological function in glioma remains unknown. In the present study, lnc-NLC1-C expression was detected using reverse transcription-quantitative (RT-q)PCR in U251, SHG44, U87MG and U118MG glioma cells. U87MG cells were transfected with lnc-NLC1-C overexpression or interference vectors. Cell proliferation was detected using a Cell Counting Kit-8 assay. Cell migration and invasion were examined using a Transwell assay, while apoptosis, cell cycle and reactive oxygen species production were evaluated using flow cytometry, and the expression levels of lnc-NLC1-C, microRNA (miR)-383 and peroxiredoxin 3 (PRDX-3) were measured using western blotting and RT-qPCR. Rescue experiments were performed to verify the function of the lnc-NLC1-C/miR-383/PRDX-3 axis. The highest expression levels of lnc-NLC1-C were identified in U87MG glioma cells. Overexpression of lnc-NLC1-C expression promoted cell proliferation, G₁ phase blocking, migration and invasion, while inhibiting apoptosis and autophagy in U87MG cells. Mechanistically, miR-383 could bind to lnc-NLC1-C to regulate PRDX-3 expression and improve its oncogenic effect. Rescue experiments confirmed that the lnc-NLC1-C/miR-383/PRDX-3 axis was involved in the molecular mechanism of glioma progression. Therefore, lnc-NLC1-C may be a tumor promoter that affects multiple biological functions, such as migration, invasion and autophagy, in glioma cells.

SUBMITTER: Xu Z

PROVIDER: S-EPMC8299021 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundThe present study is aimed at exploring the specific expression of miR-193a-3p and the mechanism underlying miR-193a-3p-mediated mesenchymal transition (MT), invasion, and migration in glioma.MethodsThe gene expression profile datasets of GSE39486 and GSE25676 were downloaded from the National Center for Biotechnology (NCBI). Data regarding the expression of miR-193a-3p and survival curves were derived from Chinese Glioma Genome Atlas (CGGA). Online websites including miRWalk, DIANA, and starbase were employed to predict the target genes for miR-193a-3p. The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed by the Omicsbean online software. Module analysis of the protein-protein interaction (PPI) networks was performed by the plug-in Molecular Complex Detection (MCODE), and the degrees of genes were calculated by CytoHubba plug-in of Cytoscape. Survival curves were based on the Gene Expression Profile Interaction Analysis (GEPIA). Transwell, wound healing, and Western blot experiments were performed to investigate the effects of miR-193a-3p and beta-transducin repeat containing E3 ubiquitin protein ligase (BTRC) on the invasion, migration, and MT of glioma.ResultsmiR-193a-3p was highly expressed in glioma tissues and significantly correlated with poor survival in patients with glioma. The target genes for miR-193a-3p were involved in many cancer-related signaling pathways. The PPI showed 11 genes with both high degrees and MCODE scores in the network. Survival analysis demonstrated that the expression of BTRC was significantly correlated with the prognosis of patients with glioma. The results from the transwell, wound healing, and Western blot analyses suggested that miR-193a-3p promoted the invasion, migration, and MT of glioma cells, which could be reversed by BTRC.ConclusionsmiR-193a-3p was upregulated in patients with glioma and could affect the invasion, migration, and MT of glioma by regulating BTRC.

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Lnc-NLC1-C inhibits migration, invasion and autophagy of glioma cells by targeting miR-383 and regulating PRDX-3 expression.

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